Abstract
In experimental models of brain injury of the ischemia-reperfusion type, there is a period of time in which the formation of oxidative damage exceeds its repair. Simultaneously, the expression of immediate early genes is induced to activate the expression of late effector genes. Drugs that reduce the need to repair during this transient period of time also attenuate neuronal death after brain injury. An example discussed in this review is the activator protein-1 (AP-1), the product of the c-fos gene and other immediate early genes. What is the effect of a delayed expression of these genes in relationship to the process of cell death? This short period presents a window of opportunity to study the effects of oxidative damage on gene expression in the brain and specific deficiencies in gene repair that have been associated with particular neurological disorders.
